<<snip>>
We report the identification of a modified variant of the Rieske
iron-sulfur protein
<<snip>>

Epilepsia. 2005 Mar;46(3):339-43. Related Articles, Links

Proteomic identification of the involvement of the mitochondrial rieske
protein in epilepsy.

Junker H, Spate K, Suofu Y, Walther R, Schwarz G, Kammer W, Nordheim A,
Walker LC, Runge U, Kessler C, Popa-Wagner A.

Department of Neurology, Ernst-Moritz-Arndt-University, Greifswald,
Germany.

Summary: Purpose: Kindled seizures are widely used to model
epileptogenesis, but the molecular mechanisms underlying the attainment
of kindling status are largely unknown. Recently we showed that
achievement of kindling status in the Sprague-Dawley rat is associated
with a critical developmental interval of 25 +/- 1 days; the
identification of this long, well-defined developmental interval for
inducing kindling status makes possible a dissection of the cellular
and genetic events underlying this phenomenon and its relation to
normal and pathologic brain function. Methods: By using proteomics on
cerebral tissue from our new rat kindling model, we undertook a global
analysis of protein expression in kindled animals. Some of the
identified proteins were further investigated by using
immunohistochemistry. Results: We report the identification of a
modified variant of the Rieske iron-sulfur protein, a component of the
mitochondrial cytochrome bc1 complex, whose isoelectric point is
shifted toward more alkaline values in the hippocampus of kindled rats.
By immunohistochemistry, the Rieske protein is well expressed in the
hippocampus, except in the CA1 subfield, an area of selective
vulnerability to seizures in humans and animal models. We also noted an
asymmetric, selective expression of the Rieske protein in the
subgranular neurons of the dorsal dentate gyrus, a region implicated in
neurogenesis. Conclusions: These results indicate that the Rieske
protein may play a role in the response of neurons to seizure activity
and could give important new insights into the molecular pathogenesis
of epilepsy.

PMID: 15730530 [PubMed - in process]

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